Yajima Y, Akita Y, Yamaguchi A, Saito T
Department of Tumor Cell Biology, Tokyo Metropolitan Institute of Medical Science, Japan.
Biochem Biophys Res Commun. 1990 Dec 14;173(2):571-7. doi: 10.1016/s0006-291x(05)80073-7.
Thyrotropin-releasing hormone (TRH) stimulates biphasic prolactin (PRL) secretion from rat pituitary GH3 cells. The pretreatment of cells with EGTA (100 microM) plus arachidonic acid (15 microM), a condition which decreased TRH-responsive intracellular Ca2+ pools, eliminated the activity of TRH on burst PRL secretion (2 min) but did not alter that on sustained PRL secretion (30 min). However, the treatment of cells with EGTA, arachidonic acid and H-7 (300 microM), a potent inhibitor of protein kinase C (PKC), almost completely suppressed the activity of TRH for sustained PRL secretion. In cells down-modulated for PKC, TRH abolished this Ca2(+)-independent sustained PRL secretion. These results suggest that TRH acts through a separate, Ca2(+)-independent secretory mechanism, besides by modulating the Ca2(+)-dependent mechanism and that PKC is involved in this Ca2(+)-independent secretory pathway.
促甲状腺激素释放激素（TRH）刺激大鼠垂体GH3细胞分泌双相催乳素（PRL）。用乙二醇双四乙酸（EGTA，100微摩尔）加花生四烯酸（15微摩尔）预处理细胞，这种处理会减少TRH反应性细胞内钙离子池，消除了TRH对PRL爆发性分泌（2分钟）的活性，但未改变其对PRL持续性分泌（30分钟）的活性。然而，用EGTA、花生四烯酸和H - 7（300微摩尔，一种蛋白激酶C（PKC）的强效抑制剂）处理细胞，几乎完全抑制了TRH对PRL持续性分泌的活性。在PKC下调的细胞中，TRH消除了这种不依赖钙离子的PRL持续性分泌。这些结果表明，TRH除了通过调节依赖钙离子的机制外，还通过一种独立的、不依赖钙离子的分泌机制起作用，并且PKC参与了这种不依赖钙离子的分泌途径。
